Insulin-like growth factor-1 (IGF-1)-induced inhibition of growth hormone secretion is associated with sleep suppression

• Published in: Brain research 1999-02, Vol.818 (2), p.267-274
• Main Authors: Obál, F., Kapás, L., Gardi, J., Taishi, P., Bodosi, B., Krueger, J.M.
• Format: Article
• Language: English
• Subjects: Analysis of Variance; Animals; Biological and medical sciences; Dose-Response Relationship, Drug; Drug Evaluation, Preclinical; EEG; Electroencephalography; Feedback; Fundamental and applied biological sciences. Psychology; GHRH; Growth hormone; Human Growth Hormone - metabolism; IGF-1; Injections, Intraventricular; Insulin-Like Growth Factor I - pharmacology; Male; Rabbits; Rats; Rats, Sprague-Dawley; Secretory Rate - drug effects; Sleep; Sleep - drug effects; Sleep. Vigilance; Somatostatin; Vertebrates: nervous system and sense organs
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(98)01286-4

The hypothalamic growth hormone (GH)-releasing hormone (GHRH) promotes non-rapid eye movement sleep (NREMS). Insulin-like growth factor-1 (IGF-1) acts as a negative feedback in the somatotropic axis inhibiting GHRH and stimulating somatostatin. To determine whether this feedback alters sleep, rats and rabbits were injected intracerebroventricularly (i.c.v.) with IGF-1 (5.0 and 0.25 μg, respectively) and the sleep–wake activity was studied. Compared to baseline (i.c.v. injection of physiological saline), IGF-1 elicited prompt suppressions in both NREMS and rapid eye movement sleep (REMS) in postinjection hour 1 in rats and rabbits. The intensity of NREMS (characterized by the slow wave activity of the EEG by means of fast-Fourier analysis) was significantly enhanced 7 to 11 h postinjection in rats. Plasma GH concentrations were measured in 30-min samples after i.c.v. IGF-1 injection in rats and a significant suppression of GH secretion was observed 30 min postinjection. The simultaneous inhibition of the somatotropic axis and sleep raises the possibility that the sleep alterations also result from an IGF-1-induced suppression of GHRH. The late increases in NREMS intensity are attributed to metabolic actions of IGF-1 or to a release of GHRH from the IGF-1-induced inhibition.